作者: Steven D. Bowden , Vinoy K. Ramachandran , Gitte M. Knudsen , Jay C. D. Hinton , Arthur Thompson
DOI: 10.1371/JOURNAL.PONE.0013871
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摘要: Background In comparison to the comprehensive analyses performed on virulence gene expression, regulation and action, intracellular metabolism of Salmonella during infection is a relatively under-studied area. We investigated role tricarboxylic acid (TCA) cycle in replication Typhimurium resting activated macrophages, epithelial cells, mice. Methodology/Principal Findings We constructed deletion mutations 5 TCA genes S. including gltA, mdh, sdhCDAB, sucAB, sucCD. found that mutants exhibited increased net murine macrophages compared wild-type. In contrast, an cell model showed ΔsucCD ΔgltA strains had reduced The glyoxylate shunt was not responsible for within macrophages. also confirmed that, model, ΔsucAB are attenuated virulence. Conclusions/Significance Our results suggest disruption increases ability survive cells non-phagocytic unlike cannot mount oxidative nitrosative defence response against pathogens; our show HeLa mutant or no change levels wild-type [1]. attenuation mice, their may encounter environments host where complete advantageous.